Alterations in early cytokine-mediated immune responses to Plasmodium falciparum infection in Tanzanian children with mineral element deficiencies: a cross-sectional survey

E.V. Mbugi, M. Meijerink, J. Veenemans, P.V. Jeurink, M. McCall, R.M. Olomi, J.F. Shao, H. Verhoef, H.F.J. Savelkoul

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Background - Deficiencies in vitamins and mineral elements are important causes of morbidity in developing countries, possibly because they lead to defective immune responses to infection. The aim of the study was to assess the effects of mineral element deficiencies on early innate cytokine responses to Plasmodium falciparum malaria. Methods - Peripheral blood mononuclear cells from 304 Tanzanian children aged 6-72 months were stimulated with P. falciparum-parasitized erythrocytes obtained from in vitro cultures. Results - The results showed a significant increase by 74% in geometric mean of TNF production in malaria-infected individuals with zinc deficiency (11% to 240%; 95% CI). Iron deficiency anaemia was associated with increased TNF production in infected individuals and overall with increased IL-10 production, while magnesium deficiency induced increased production of IL-10 by 46% (13% to 144%) in uninfected donors. All donors showed a response towards IL-1ß production, drawing special attention for its possible protective role in early innate immune responses to malaria. Conclusions - In view of these results, the findings show plasticity in cytokine profiles of mononuclear cells reacting to malaria infection under conditions of different micronutrient deficiencies. These findings lay the foundations for future inclusion of a combination of precisely selected set of micronutrients rather than single nutrients as part of malaria vaccine intervention programmes in endemic countries
Original languageEnglish
Article number130
Number of pages13
JournalMalaria Journal
Publication statusPublished - 2010



  • zinc supplementation
  • innate immunity
  • trace-elements
  • tnf-alpha
  • malaria
  • cells
  • expression
  • induction
  • monocytes
  • interleukin-12

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